Necrotizing fasciitis pathophysiology: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
All types of necrotizing fasciitis have common pathophysiology but the speed of development and associated clinical features may differ depending on the causative organisms.
Development of necrotizing fasciitis is the result of  
*The bacteria or bacterium usually transmitted into the body via
:*An external injury (surgical sites, a cut, scratch, bruise, boil, or any small injury)
:*Direct spread from a punctured / perforated internal or sexual organ (particularly the colon, rectum, or anus)
:*Sexual
*Following transmission, the bacteria or bacterium spreads via the fascia, producing [[exotoxins]] and [[endotoxins]].
*These toxins restricts blood supply to tissues ([[ischemia]]) leading to digestion of cells by enzymes resulting in a lesion consisting of pus and the fluid remains of dead tissue.
*As the blood supply to these tissues is impaired,  neither antibiotics nor the body’s own mechanisms to fight infection are able to reach these tissues.


'''Type 1 necrotizing fasciitis''' ('''Synergistic NF''')
*Comparatively slow process
*It is commonly seen in [[immunocompromised]] or those with underlying abdominal pathology
*Synergistic NF develops following complicated abdominal surgery, [[abscess|ischiorectal]] or [[abscess|perineal abscesses]] when the gut flora breaches the mucosa entering tissue planes.





Revision as of 16:06, 1 September 2016

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Overview

Pathophysiology

Development of necrotizing fasciitis is the result of


“Flesh-eating bacteria” is a misnomer, as the bacteria do not actually eat the tissue. They cause the destruction of skin and muscle by releasing toxins (virulence factors). These include streptococcal pyogenic exotoxins and other virulence factors. S. pyogenes produces an exotoxin known as a superantigen. This toxin is capable of activating T-cells non-specifically. This causes the over-production of cytokines that over-stimulate macrophages. The macrophages cause the actual tissue damage by releasing oxygen free radicals that are normally intended to destroy bacteria but are capable of damaging nearly any macromolecule they contact in the body.

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